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However, the role of macrophages in mediating endothelial function via exosomes in these inflammatory diseases remains elusive.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      Exosomes isolated from\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      (\n                      <jats:italic>P.g<\/jats:italic>\n                      )\u2010infected THP\u20101\u2010derived macrophages (\n                      <jats:italic>P.g<\/jats:italic>\n                      \u2010Exos) and uninfected macrophages (Con\u2010Exos) were verified and their effects on human umbilical vein endothelial cells (HUVECs) were investigated. The expression of TNF\u2010\u03b1 and IL\u20106 in HUVECs was tested by quantitative real time PCR (qRT\u2010PCR) and ELISA. A fluorescein isothiocyanate (FITC)\u2010dextran leakage assay and a THP\u20101 monocyte adhesion assay were used to explore vascular permeability and cellular adhesion. The migration and angiogenic capacity were evaluated using transwell, cell scratch, and tube\u2010forming assays. HUVECs were pretreated with SC79 (Akt activator) to explore the mechanism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>P.g<\/jats:italic>\n                      stimulation increased the release of exosomes from macrophages.\n                      <jats:italic>P.g<\/jats:italic>\n                      \u2010Exos inhibited HUVECs' migration and tube formation capabilities while increasing vascular permeability, promoting leukocyte adhesion and releasing proinflammatory factors. Importantly,\n                      <jats:italic>P.g<\/jats:italic>\n                      \u2010Exos induced endothelial dysfunction partially via the Akt\/mTOR pathway suppression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Summarily, this study reveals that the exosomes derived from inflammatory macrophages mediate HUVECs dysfunction partially via the Akt\/mTOR pathway, providing novel insights into potential treatments for oral inflammatory diseases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/odi.70314","type":"journal-article","created":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T04:38:13Z","timestamp":1774845493000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Exosomes of\n                    <scp>\n                      <i>Porphyromonas gingivalis<\/i>\n                    <\/scp>\n                    \u2010Infected Macrophages Impair the Endothelial Barrier and Angiogenesis In\u00a0Vitro"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7644-5079","authenticated-orcid":false,"given":"Yanling","family":"Zhou","sequence":"first","affiliation":[{"name":"Hosiptal of Stomatology, Sun Yat\u2010Sen University  Guangzhou Guangdong China"},{"name":"Guangdong Provincial Key Laboratory of Stomatology, Sun Yat\u2010Sen University  Guangzhou Guangdong China"},{"name":"Guanghua School of Stomatology, Sun Yat\u2010Sen University  Guangzhou Guangdong China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yihua","family":"Huang","sequence":"additional","affiliation":[{"name":"Hosiptal of Stomatology, Sun Yat\u2010Sen University  Guangzhou Guangdong China"},{"name":"Guangdong Provincial Key Laboratory of Stomatology, Sun Yat\u2010Sen University  Guangzhou Guangdong China"},{"name":"Guanghua School 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